本文選題：鹽酸阿霉素　切入點(diǎn)：氧化石墨烯　出處：《吉林大學(xué)》2017年碩士論文　論文類型：學(xué)位論文

【摘要】：目的:研究、探討PF127-GO-DOX抗人神經(jīng)膠質(zhì)瘤的作用及其相關(guān)分子機(jī)制,為腫瘤的信號通路分子靶向治療提供更多的證據(jù)。方法:(1)培養(yǎng)人源性膠質(zhì)瘤細(xì)胞系U251細(xì)胞:U251細(xì)胞的復(fù)蘇、培養(yǎng)與凍存;(2)比較PG、PF127-GO、DOX、PF127-GO對U251細(xì)胞凋亡的作用:實驗分為4組:模型組、PF127-GO組、DOX組、PF127-GO-DOX組,流式細(xì)胞儀檢測細(xì)胞凋亡率;(3)提取U251細(xì)胞株胞漿蛋白,Western-blotting法測定P53、細(xì)胞外信號調(diào)節(jié)蛋白激酶1/2(extracellular signal-regulated kinases 1/2,ERK1/2),c-jun氨基末端激酶/(c-Jun amino(N)-terminal kinases,JNK)、半胱氨酸的天冬氨酸蛋白水解酶-3(cysteinyl aspartate specific proteinase,Caspase-3)的表達(dá)水平。結(jié)果:(1)PF127-GO-DOX、DOX對膠質(zhì)瘤U251細(xì)胞有明顯的促凋亡作用;(2)PF127-GO-DOX可以上調(diào)P53、JNK、Caspase-3,下調(diào)ERK1/2的表達(dá)。結(jié)論:(1)PF127-GO-DOX對人膠質(zhì)瘤細(xì)胞有較強(qiáng)的促凋亡作用,且優(yōu)于單獨(dú)的DOX;(2)PF127-GO-DOX可能通過激活JNK及P53通路,抑制ERK1/2通路,誘導(dǎo)腫瘤細(xì)胞凋亡,發(fā)揮抗膠質(zhì)瘤作用。
[Abstract]:Objective: to investigate the effect of PF127-GO-DOX on human glioma and its related molecular mechanism, and to provide more evidence for the molecular targeting therapy of tumor signaling pathway. Methods: human glioma cell line U251 cell line: U251 cell line was resuscitated. The effect of PGN PF127-GOXP127-GO on apoptosis of U251 cells was compared. The experiment was divided into four groups: model group, PF127-go group, DOX group, PF127-GO-DOX group. Extracellular signal regulated protein kinase 1 / 2 extracellular signal-regulated kinases 1 / 2 ERK1 / 2 ERK1 / 2 ERK1 / 2ERK-1 / 2ERK-1 / 2ERK-1 / 2ERK-1 / 2ERK-1 / 2, c-Jun amino(N)-terminal kinaseshs / JNKK, cysteine aspartyl aspartate specific proteinase / caspase-3 (Caspase-3), cytoplasmic protein hydrolase (-3cysteinyl aspartate specific proteinase) of U251 cell line (U251 cell line) was extracted by flow cytometry (FCM) and extracellular signal regulated protein kinase (extracellular signal-regulated / kinases 1 / 2 / 2 / 2 / 2 / 2). Results PF127-GO-DOX could significantly promote apoptosis in U251 glioma cells and could up-regulate the expression of P53, JNK-Caspase-3 and down-regulate the expression of ERK1/2. Conclusion: F127-GO-DOX has a strong apoptotic effect on human glioma cells. In addition, PF127-GO-DOX may inhibit ERK1/2 pathway, induce apoptosis of tumor cells and play an anti-glioma role by activating JNK and p53 pathway.
【學(xué)位授予單位】：吉林大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2017
【分類號】：R739.41

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